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NEUROLOGY 2004;62:1894-1896
© 2004 American Academy of Neurology
Brief Communications

Anti-ryanodine receptor antibodies and FK506 in myasthenia gravis

M. Takamori, MD, M. Motomura, MD, N. Kawaguchi, MD, Y. Nemoto, MD, T. Hattori, MD, H. Yoshikawa, MD and K. Otsuka, PhD

From the Neurological Center (Drs. Takamori and Otsuka), Kanazawa-Nishi Hospital, Kanazawa; Department of Internal Medicine (Dr. Motomura), Nagasaki University Hospital; Department of Neurology (Drs. Kawaguchi, Nemoto, and Hattori), Chiba University Hospital; and Department of Neurology (Dr. Yoshikawa), Kanazawa University Hospital, Japan.

Address correspondence and reprint requests to Dr. Masaharu Takamori, Neurological Center, Kanazawa-Nishi Hospital, 6–15–41, Ekinishi-honmachi, Kanazawa 920–0025, Japan; e-mail: t-kiyomi{at}guitar.ocn.ne.jp

Anti-ryanodine receptor (RyR) antibodies were measured in sera from 33 myasthenia gravis (MG) patients using three peptides from the human RyR1 sequence, two C-terminal peptides included in the functional calcium release channel, and an N-terminal peptide implicated in ion-conduction. Antibodies were more frequently positive against the two C-terminal peptides, particularly in thymoma-associated MG. In a preliminary open trial with FK506, immunosuppressant and enhancer of RyR-related sarcoplasmic calcium release, the authors observed the sustained benefits in anti-RyR-positive MG patients.

Received September 25, 2003. Accepted in final form January 28, 2004.






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